Lawler J E, Cox R H
Pavlov J Biol Sci. 1985 Jul-Sep;20(3):101-15. doi: 10.1007/BF03003593.
While many studies have attempted to produce hypertension through the use of various environmental stressors, few have succeeded in producing chronic elevations in blood pressure beyond levels considered to be borderline hypertensive (140-160 mm Hg systolic). The problem with most studies stems from the use of genetically normotensive animals and the selection of stressors to which animals readily adapt. A new approach is suggested, which recognizes the role of genetics in human essential hypertension. Animals with one hypertensive parent do not develop spontaneous hypertension but show a more sensitive cardiovascular response to environmental stressors than animals with normotensive parents. Preliminary studies revealed that animals with a mixed genetic history of hypertension develop spontaneous borderline hypertension. When subjected to shock-shock conflict, these borderline hypertensive rats (BHR) developed permanent hypertension that failed to abate even after a ten-week, shock-free recovery period. The hypertension was accompanied by elevated heart weight to body weight ratios and by significant cardiac pathology. Subsequent work has demonstrated that these animals also become hypertensive when fed a high-sodium diet. Finally, in a series of exercise studies, we found that BHRs subjected to a shock stressor were protected against stress-induced hypertension if they exercised daily. The potential of this model for studies of the mechanisms by which environmental variables produce permanent hypertension is discussed.
虽然许多研究试图通过使用各种环境应激源来诱发高血压,但很少有研究能够成功使血压持续升高到超过临界高血压水平(收缩压140 - 160毫米汞柱)。大多数研究的问题在于使用了基因正常血压的动物,以及选择了动物容易适应的应激源。有人提出了一种新方法,该方法认识到遗传学在人类原发性高血压中的作用。有一个高血压亲本的动物不会自发产生高血压,但与有正常血压亲本的动物相比,它们对环境应激源表现出更敏感的心血管反应。初步研究表明,具有混合高血压遗传史的动物会出现自发的临界高血压。当遭受休克 - 休克冲突时,这些临界高血压大鼠(BHR)会发展为永久性高血压,即使在经过为期十周的无休克恢复期后,血压仍未下降。高血压伴随着心脏重量与体重比值的升高以及明显的心脏病理变化。后续研究表明,这些动物在喂食高钠饮食时也会患上高血压。最后,在一系列运动研究中,我们发现,如果每天进行运动,遭受休克应激源的BHR可以预防应激诱导的高血压。本文讨论了该模型在研究环境变量导致永久性高血压机制方面的潜力。